دورية أكاديمية
NECAB2 is an endosomal protein important for striatal function.
| العنوان: | NECAB2 is an endosomal protein important for striatal function. |
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| المؤلفون: | Bueno D; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Germany. Electronic address: diones.bueno@gmail.com., Narayan Dey P; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Germany. Electronic address: pndey85@gmail.com., Schacht T; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Germany. Electronic address: teresa.84.boldt@gmail.com., Wolf C; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Germany. Electronic address: wolf.christina90@gmail.com., Wüllner V; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Germany. Electronic address: verena.wuellner@gmail.com., Morpurgo E; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Germany. Electronic address: elena.morpurgo@gmail.com., Rojas-Charry L; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Germany; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Anatomy, Germany. Electronic address: lilianarojasch0211@gmail.com., Sessinghaus L; University Medical Center of the Johannes Gutenberg-University Mainz, Institute of Neuropathology, Germany. Electronic address: lena_sessinghaus@web.de., Leukel P; University Medical Center of the Johannes Gutenberg-University Mainz, Institute of Neuropathology, Germany. Electronic address: Petra.Leukel@unimedizin-mainz.de., Sommer C; University Medical Center of the Johannes Gutenberg-University Mainz, Institute of Neuropathology, Germany. Electronic address: clemens.sommer@unimedizin-mainz.de., Radyushkin K; University Medical Center of the Johannes Gutenberg-University Mainz, Mouse Behavior Unit, Germany. Electronic address: radyushkin@uni-mainz.de., Florin L; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Virology, Germany. Electronic address: lflorin@uni-mainz.de., Baumgart J; University Medical Center of the Johannes Gutenberg-University Mainz, Translational Animal Research Center (TARC), Germany. Electronic address: jan.baumgart@unimedizin-mainz.de., Stamm P; University Medical Center of the Johannes Gutenberg-University Mainz, Center for Cardiology, Germany. Electronic address: PaulStamm@gmx.de., Daiber A; University Medical Center of the Johannes Gutenberg-University Mainz, Center for Cardiology, Germany. Electronic address: daiber@uni-mainz.de., Horta G; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Anatomy, Germany. Electronic address: guihorta@uni-mainz.de., Nardi L; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Anatomy, Germany. Electronic address: leonardi@uni-mainz.de., Vasic V; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Anatomy, Germany. Electronic address: vasic@uni-mainz.de., Schmeisser MJ; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Anatomy, Germany. Electronic address: mschmeisser@uni-mainz.de., Hellwig A; Department of Neurobiology, Interdisciplinary Center for Neurosciences (IZN), Heidelberg University, Germany. Electronic address: Hellwig@nbio.uni-heidelberg.de., Oskamp A; Institute of Neuroscience and Medicine (INM-2), Forschungszentrum Jülich GmbH, Germany. Electronic address: a.oskamp@fz-juelich.de., Bauer A; Institute of Neuroscience and Medicine (INM-2), Forschungszentrum Jülich GmbH, Germany. Electronic address: an.bauer@fz-juelich.de., Anand R; Institute of Biochemistry and Molecular Biology I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Electronic address: Ruchika.Anand@uni-duesseldorf.de., Reichert AS; Institute of Biochemistry and Molecular Biology I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Electronic address: reichert@hhu.de., Ritz S; Institute of Molecular Biology gGmbH (IMB), Mainz, Germany. Electronic address: S.Ritz@imb-mainz.de., Nocera G; Institute of Developmental Biology and Neurobiology, Johannes Gutenberg-University Mainz, Germany. Electronic address: gnocera@uni-mainz.de., Jacob C; Institute of Developmental Biology and Neurobiology, Johannes Gutenberg-University Mainz, Germany. Electronic address: cjacob@uni-mainz.de., Peper J; Institute of Developmental Biology and Neurobiology, Johannes Gutenberg-University Mainz, Germany. Electronic address: jopeper@uni-mainz.de., Silies M; Institute of Developmental Biology and Neurobiology, Johannes Gutenberg-University Mainz, Germany. Electronic address: msilies@uni-mainz.de., Frauenknecht KBM; University Medical Center of the Johannes Gutenberg-University Mainz, Institute of Neuropathology, Germany; Institute of Neuropathology, University and University Hospital Zurich, Switzerland. Electronic address: frauenknechtk@gmail.com., Schäfer MKE; Department of Anesthesiology, University Medical Center of the Johannes Gutenberg-University Mainz, Germany. Electronic address: michael.schaefer@unimedizin-mainz.de., Methner A; University Medical Center of the Johannes Gutenberg-University Mainz, Institute for Molecular Medicine, Germany. Electronic address: axel.methner@gmail.com. |
| المصدر: | Free radical biology & medicine [Free Radic Biol Med] 2023 Nov 01; Vol. 208, pp. 643-656. Date of Electronic Publication: 2023 Sep 16. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Science Country of Publication: United States NLM ID: 8709159 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-4596 (Electronic) Linking ISSN: 08915849 NLM ISO Abbreviation: Free Radic Biol Med Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Tarrytown, NY : Elsevier Science Original Publication: New York : Pergamon, c1987- |
| مواضيع طبية MeSH: | Antioxidants*/metabolism , Oxidative Stress*/physiology , Corpus Striatum*/physiology, Animals ; Mice ; Calcium-Binding Proteins/metabolism ; Eye Proteins/metabolism ; Mice, Knockout ; Mitochondria/genetics ; Mitochondria/metabolism ; Neurons/metabolism ; Oxidation-Reduction |
| مستخلص: | Synaptic signaling depends on ATP generated by mitochondria. Dysfunctional mitochondria shift the redox balance towards a more oxidative environment. Due to extensive connectivity, the striatum is especially vulnerable to mitochondrial dysfunction. We found that neuronal calcium-binding protein 2 (NECAB2) plays a role in striatal function and mitochondrial homeostasis. NECAB2 is a predominantly endosomal striatal protein which partially colocalizes with mitochondria. This colocalization is enhanced by mild oxidative stress. Global knockout of Necab2 in the mouse results in increased superoxide levels, increased DNA oxidation and reduced levels of the antioxidant glutathione which correlates with an altered mitochondrial shape and function. Striatal mitochondria from Necab2 knockout mice are more abundant and smaller and characterized by a reduced spare capacity suggestive of intrinsic uncoupling respectively mitochondrial dysfunction. In line with this, we also found an altered stress-induced interaction of endosomes with mitochondria in Necab2 knockout striatal cultures. The predominance of dysfunctional mitochondria and the pro-oxidative redox milieu correlates with a loss of striatal synapses and behavioral changes characteristic of striatal dysfunction like reduced motivation and altered sensory gating. Together this suggests an involvement of NECAB2 in an endosomal pathway of mitochondrial stress response important for striatal function. Competing Interests: Declaration of competing interest The authors declare no competing interest. (Copyright © 2023 Elsevier Inc. All rights reserved.) |
| المشرفين على المادة: | 0 (Antioxidants) 0 (Calcium-Binding Proteins) 0 (Eye Proteins) 0 (NECAB2 protein, mouse) |
| تواريخ الأحداث: | Date Created: 20230918 Date Completed: 20231103 Latest Revision: 20231103 |
| رمز التحديث: | 20240628 |
| DOI: | 10.1016/j.freeradbiomed.2023.09.003 |
| PMID: | 37722569 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1873-4596 |
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| DOI: | 10.1016/j.freeradbiomed.2023.09.003 |